title: Meta-analyses of vitamin D intake, 25-hydroxyvitamin D status, vitamin D receptor polymorphisms, and colorectal cancer risk.
abstract: BACKGROUND
  Our objective was to conduct a systematic review and meta-analysis of prospective studies on colorectal cancer (CRC) and vitamin D intake and 25-hydroxyvitamin D status, as part of the World Cancer Research Fund Continuous Update Project. We also aimed at conducting meta-analysis of all studies on CRC and vitamin D receptor (VDR) single-nucleotide polymorphisms.
  
  
  METHODS
  Relevant studies were identified in PubMed (up to June 2010). Inclusion criteria were original and peer-reviewed publications with a prospective design (for studies on vitamin D intake or status). Random effects of dose-response meta-analyses were performed on cancer incidence.
  
  
  RESULTS
  We observed inverse associations of CRC risk with dietary vitamin D [summary relative risk (RR) per 100 IU/day = 0.95, 95% CI: 0.93-0.98; 10 studies; range of intake (midpoints) = 39-719 IU/day] and serum/plasma 25-hydroxyvitamin D (RR per 100 IU/L = 0.96, 0.94-0.97; 6 studies; range = 200-1,800 IU/L), but not with total vitamin D (5 studies). Supplemental (2 studies; range = 0-600 IU/day) and total (4 studies; range = 79-732 IU/day) vitamin D intake and 25-hydroxyvitamin D status (6 studies; range = 200-1,800 IU/L) were inversely associated with colon cancer risk. We did not observe statistically significant associations between FokI, PolyA, TaqI, Cdx2, and ApaI VDR polymorphisms and CRC risk. The BsmI polymorphism was associated with a lower CRC risk (RR = 0.57, 0.36-0.89 for BB versus bb, 8 studies).
  
  
  CONCLUSIONS
  These meta-analyses support the evidence of an inverse association between vitamin D intake, 25-hydroxyvitamin D status, and the BsmI VDR polymorphism and CRC risk.
  
  
  CONCLUSIONS
  Improving vitamin D status could be potentially beneficial against CRC incidence.
authors.affiliation: Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK. m.touvier@imperial.ac.uk
authors.forename: Mathilde
authors.initials: M
authors.lastname: Touvier
authors.forename: Doris S M
authors.initials: DS
authors.lastname: Chan
authors.forename: Rosa
authors.initials: R
authors.lastname: Lau
authors.forename: Dagfinn
authors.initials: D
authors.lastname: Aune
authors.forename: Rui
authors.initials: R
authors.lastname: Vieira
authors.forename: Darren C
authors.initials: DC
authors.lastname: Greenwood
authors.forename: Ellen
authors.initials: E
authors.lastname: Kampman
authors.forename: Elio
authors.initials: E
authors.lastname: Riboli
authors.forename: Serge
authors.initials: S
authors.lastname: Hercberg
authors.forename: Teresa
authors.initials: T
authors.lastname: Norat
mesh_terms: D016022:Case-Control Studies; D015179:Colorectal Neoplasms / Q000097:blood / Q000209:etiology* / Q000517:prevention & control; D005838:Genotype; D006801:Humans; D015994:Incidence; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D011379:Prognosis; D011446:Prospective Studies; D018167:Receptors, Calcitriol / Q000235:genetics*; D012307:Risk Factors; D014807:Vitamin D / Q000008:administration & dosage* / Q000031:analogs & derivatives* / Q000097:blood
chemical_list: D018167:Receptors, Calcitriol; D014807:Vitamin D; C104450:25-hydroxyvitamin D